Ethanol Alters Cell Fate of Fetal Human Brain-Derived Stem and Progenitor Cells

2010 ◽  
Vol 34 (9) ◽  
pp. 1574-1583 ◽  
Author(s):  
Sharada D. Vangipuram ◽  
William D. Lyman
Keyword(s):  
Human Brain ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Stem And Progenitor Cells

scholarly journals The Making of Hematopoiesis: Developmental Ancestry and Environmental Nurture

2018 ◽  
Vol 19 (7) ◽  
pp. 2122 ◽  
Author(s):  
Geoffrey Brown ◽  
Rhodri Ceredig ◽  
Panagiotis Tsapogas
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Hematopoietic Stem ◽  
Fate Determination ◽  
Intermediate Progenitors ◽  
Lineage Tree ◽  
Stem And Progenitor Cells ◽  
The Many

Evidence from studies of the behaviour of stem and progenitor cells and of the influence of cytokines on their fate determination, has recently led to a revised view of the process by which hematopoietic stem cells and their progeny give rise to the many different types of blood and immune cells. The new scenario abandons the classical view of a rigidly demarcated lineage tree and replaces it with a much more continuum-like view of the spectrum of fate options open to hematopoietic stem cells and their progeny. This is in contrast to previous lineage diagrams, which envisaged stem cells progressing stepwise through a series of fairly-precisely described intermediate progenitors in order to close down alternative developmental options. Instead, stem and progenitor cells retain some capacity to step sideways and adopt alternative, closely related, fates, even after they have “made a lineage choice.” The stem and progenitor cells are more inherently versatile than previously thought and perhaps sensitive to lineage guidance by environmental cues. Here we examine the evidence that supports these views and reconsider the meaning of cell lineages in the context of a continuum model of stem cell fate determination and environmental modulation.

scholarly journals Epigenetic profiles signify cell fate plasticity in unipotent spermatogonial stem and progenitor cells

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Ying Liu ◽  
Eugenia G. Giannopoulou ◽  
Duancheng Wen ◽  
Ilaria Falciatori ◽  
Olivier Elemento ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Stem And Progenitor Cells

scholarly journals Fatty acid β-oxidation is required for the differentiation of larval hematopoietic progenitors in Drosophila

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Satish Kumar Tiwari ◽  
Ashish Ganeshlalji Toshniwal ◽  
Sudip Mandal ◽  
Lolitika Mandal
Keyword(s):  
Fatty Acid ◽  
Histone Acetylation ◽  
Progenitor Cells ◽  
Cell Fate ◽  
The State ◽  
Acid Oxidation ◽  
Hematopoietic Organ ◽  
Jun Kinase ◽  
Stem And Progenitor Cells ◽  
Rate Limiting

Cell-intrinsic and extrinsic signals regulate the state and fate of stem and progenitor cells. Recent advances in metabolomics illustrate that various metabolic pathways are also important in regulating stem cell fate. However, our understanding of the metabolic control of the state and fate of progenitor cells is in its infancy. Using Drosophila hematopoietic organ: lymph gland, we demonstrate that Fatty Acid Oxidation (FAO) is essential for the differentiation of blood cell progenitors. In the absence of FAO, the progenitors are unable to differentiate and exhibit altered histone acetylation. Interestingly, acetate supplementation rescues both histone acetylation and the differentiation defects. We further show that the CPT1/whd (withered), the rate-limiting enzyme of FAO, is transcriptionally regulated by Jun-Kinase (JNK), which has been previously implicated in progenitor differentiation. Our study thus reveals how the cellular signaling machinery integrates with the metabolic cue to facilitate the differentiation program.

scholarly journals Helios represses megakaryocyte priming in hematopoietic stem and progenitor cells

2021 ◽  
Vol 218 (10) ◽  
Author(s):  
Giovanni Cova ◽  
Chiara Taroni ◽  
Marie-Céline Deau ◽  
Qi Cai ◽  
Vincent Mittelheisser ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Transcriptional Activators ◽  
Cell Stage ◽  
Hematopoietic Stem ◽  
Chromatin Compaction ◽  
Cell Fate Decisions ◽  
Quiescent Cells ◽  
Stem And Progenitor Cells ◽  
Expression Program

Our understanding of cell fate decisions in hematopoietic stem cells is incomplete. Here, we show that the transcription factor Helios is highly expressed in murine hematopoietic stem and progenitor cells (HSPCs), where it is required to suppress the separation of the platelet/megakaryocyte lineage from the HSPC pool. Helios acts mainly in quiescent cells, where it directly represses the megakaryocyte gene expression program in cells as early as the stem cell stage. Helios binding promotes chromatin compaction, notably at the regulatory regions of platelet-specific genes recognized by the Gata2 and Runx1 transcriptional activators, implicated in megakaryocyte priming. Helios null HSPCs are biased toward the megakaryocyte lineage at the expense of the lymphoid and partially resemble cells of aging animals. We propose that Helios acts as a guardian of HSPC pluripotency by continuously repressing the megakaryocyte fate, which in turn allows downstream lymphoid priming to take place. These results highlight the importance of negative and positive priming events in lineage commitment.

Neural Stem and Progenitor Cells: Lineage and Cell Fate Determination

2006 ◽  
pp. 55-93
Author(s):  
Stephen N. Sansom ◽  
Sabhi Rahman ◽  
Uruporn Thammongkol ◽  
Frederick J. Livesey
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Fate Determination ◽  
Stem And Progenitor Cells

scholarly journals Stem Cells and the Differentiation Hierarchy in Mammary Gland Development

2020 ◽  
Vol 100 (2) ◽  
pp. 489-523 ◽  
Author(s):  
Nai Yang Fu ◽  
Emma Nolan ◽  
Geoffrey J. Lindeman ◽  
Jane E. Visvader
Keyword(s):  
Stem Cells ◽  
Mammary Gland ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Large Scale ◽  
Mammary Epithelium ◽  
Mammary Stem ◽  
Stem And Progenitor Cells ◽  
Intrinsic Complexity ◽  
Small Pool

The mammary gland is a highly dynamic organ that undergoes profound changes within its epithelium during puberty and the reproductive cycle. These changes are fueled by dedicated stem and progenitor cells. Both short- and long-lived lineage-restricted progenitors have been identified in adult tissue as well as a small pool of multipotent mammary stem cells (MaSCs), reflecting intrinsic complexity within the epithelial hierarchy. While unipotent progenitor cells predominantly execute day-to-day homeostasis and postnatal morphogenesis during puberty and pregnancy, multipotent MaSCs have been implicated in coordinating alveologenesis and long-term ductal maintenance. Nonetheless, the multipotency of stem cells in the adult remains controversial. The advent of large-scale single-cell molecular profiling has revealed striking changes in the gene expression landscape through ontogeny and the presence of transient intermediate populations. An increasing number of lineage cell-fate determination factors and potential niche regulators have now been mapped along the hierarchy, with many implicated in breast carcinogenesis. The emerging diversity among stem and progenitor populations of the mammary epithelium is likely to underpin the heterogeneity that characterizes breast cancer.

scholarly journals Next generation of ALDH substrates and their potential to study maturational lineage biology in stem and progenitor cells

2015 ◽  
Vol 308 (7) ◽  
pp. G573-G578 ◽  
Author(s):  
Laurent Dollé ◽  
Luke Boulter ◽  
Isabelle A. Leclercq ◽  
Leo A. van Grunsven
Keyword(s):  
Stem Cells ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Cell Phenotype ◽  
Tissue Cell ◽  
Aldh Activity ◽  
Fluorescent Substrate ◽  
Metabolic Role ◽  
Stem And Progenitor Cells ◽  
Active Research

High aldehyde dehydrogenase (ALDH) activity is a feature of stem cells from normal and cancerous tissues and a reliable universal marker used to isolate them. There are numerous ALDH isoforms with preferred substrate specificity variably expressed depending on tissue, cell type, and organelle and cell status. On the other hand, a given substrate may be metabolized by several enzyme isoforms. Currently ALDH activity is evidenced by using Aldefluor, a fluorescent substrate likely to be metabolized by numerous ALDH isoforms. Therefore, isolation techniques based on ALDH activity detection select a heterogeneous population of stem or progenitor cells. Despite active research in the field, the precise role(s) of different ALDH isoforms in stem cells remains enigmatic. Understanding the metabolic role of different ALDH isoform in the control of stem cell phenotype and cell fate during development, tissue homeostasis, or repair, as well as carcinogenesis, should open perspectives to significant discoveries in tissue biology. In this perspective, novel ALDH substrates are being developed. Here we describe how new substrates could be instrumental for better isolation of cell population with stemness potential and for defining hierarchy of cell populations in tissue. Finally, we speculate on other potential applications.

scholarly journals Predictive Functions of H3K27me3 and H4K20me3 in Primate Hippocampal Stem and Progenitor Cells

2021 ◽  
Author(s):  
Christopher Rhodes ◽  
Chin Hsing Annie Lin
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Gene Activation ◽  
Protective Mechanism ◽  
Histone 3 ◽  
Stem And Progenitor Cells ◽  
Predictive Functions ◽  
Human Primate ◽  
Genomic Similarity

Epigenetic regulations play important roles in cell fate determination during neurogenesis, a process by which different types of neurons are generated from neural stem and progenitor cells (NSPCs). Although some epigenetic changes are part of developmental and aging processes, the role of tri-methylation on histone 3 lysine 27 (H3K27me3) and histone 4 lysine 20 (H4K20me3) in primate hippocampal NSPCs remains elusive. This task is best assessed within a context resembling the human brain. As more studies emerge, the baboon represents an excellent model of human central nervous system in addition to their genomic similarity. With a focus on H3K27me3 and H4K20me3, the overarching goal of this work is to reveal their respective epigenetic landscapes in NSPCs of non-human primate baboon hippocampus. We identified putative targets of H3K27me3 and H4K20me3 that suggests a protective mechanism by dual H3K27me3/H4K20me3-mediated repression of specific-lineage gene activation important for differentiation processes while controlling the progression of the cell cycle.

scholarly journals SPT6 promotes epidermal differentiation and blockade of an intestinal-like phenotype through control of transcriptional elongation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jingting Li ◽  
Xiaojun Xu ◽  
Manisha Tiwari ◽  
Yifang Chen ◽  
Mackenzie Fuller ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Transcription Elongation ◽  
Somatic Tissue ◽  
Epidermal Differentiation ◽  
Transcriptional Elongation ◽  
Adult Tissue ◽  
Proliferation And Differentiation ◽  
Stem And Progenitor Cells ◽  
Active Investigation

AbstractIn adult tissue, stem and progenitor cells must tightly regulate the balance between proliferation and differentiation to sustain homeostasis. How this exquisite balance is achieved is an area of active investigation. Here, we show that epidermal genes, including ~30% of induced differentiation genes already contain stalled Pol II at the promoters in epidermal stem and progenitor cells which is then released into productive transcription elongation upon differentiation. Central to this process are SPT6 and PAF1 which are necessary for the elongation of these differentiation genes. Upon SPT6 or PAF1 depletion there is a loss of human skin differentiation and stratification. Unexpectedly, loss of SPT6 also causes the spontaneous transdifferentiation of epidermal cells into an intestinal-like phenotype due to the stalled transcription of the master regulator of epidermal fate P63. Our findings suggest that control of transcription elongation through SPT6 plays a prominent role in adult somatic tissue differentiation and the inhibition of alternative cell fate choices.

scholarly journals Chronic Interleukin-1 exposure triggers selective expansion of Cebpa-deficient multipotent hematopoietic progenitors

2020 ◽  
Author(s):  
Kelly C. Higa ◽  
Andrew Goodspeed ◽  
James S. Chavez ◽  
Vadym Zaberezhnyy ◽  
Jennifer L. Rabe ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Interleukin 1 ◽  
Myeloproliferative Neoplasm ◽  
Interleukin 1Β ◽  
Dependent Manner ◽  
Hematopoietic Stem ◽  
Hematologic Disorders ◽  
Cell Fate Decisions ◽  
Stem And Progenitor Cells

AbstractThe early events that drive hematologic disorders like clonal hematopoiesis, myelodysplastic syndrome, myeloproliferative neoplasm, and acute myeloid leukemia are not well understood. Most studies focus on the cell-intrinsic genetic changes that occur in these disorders and how they impact cell fate decisions. We consider how chronic exposure to the pro-inflammatory cytokine, interleukin-1β (IL-1β), impacts Cebpa-deficient hematopoietic stem and progenitor cells (HSPC) in competitive settings. We surprisingly found that Cebpa-deficient HSPC did not have a hematopoietic cell intrinsic competitive advantage; rather chronic IL-1β exposure engendered potent selection for Cebpa loss. Chronic IL-1β augments myeloid lineage output by activating differentiation and repressing stem cell gene expression programs in a Cebpa-dependent manner. As a result, Cebpa-deficient HSPC are resistant to the pro-differentiative effects of chronic IL-1β, and competitively expand. These findings have important implications for the earliest events that drive hematologic disorders, suggesting that chronic inflammation could be an important driver of leukemogenesis and a potential target for intervention.SummaryHiga et al. show that chronic interleukin-1β exposure primes hematopoietic stem and progenitor cells for myelopoiesis by upregulating myeloid differentiation programs and repressing stem gene programs in a Cebpa-dependent manner. Consequently, interleukin-1 potently selects for Cebpa loss in hematopoietic stem and progenitor cells.

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